It's the kind of nightmare parents dread. Morning dawns like any other, accompanied by the usual rush. The kids reach the school bus in the nick of time. Your youngest, just 18 months old, remains in his highchair, clamouring for attention. You play happily together, but by lunchtime you notice he is flushed and restless. As you put him down for his afternoon nap, his temperature has risen and he has become feverish. The usual remedies don't seem to be working and after a couple of hours you become anxious. The symptoms have worsened and you decide to act.

The doctors take samples, run their tests; their faces are grave. You are joined at the hospital by the rest of your family, watching helplessly. By bedtime, your healthy, happy child is lost for ever. How can things have changed so quickly?

Meningitis can kill its victims in just four hours. Symptoms vary; often the telltale rash does not appear and the only signs of illness are a fever and headache. The most severe form of meningitis is caused by the bacterium Neisseria meningitidis, the meningococcus. It is not rare: it lives in the nose and throat of up to 40% of the population. These hosts suffer no ill effects, but pass the bacterium on to others by coughing and sneezing, or kissing.

The trouble begins when the bacteria force their way through the tissues in the nose and throat, aiming for the bloodstream. They use the network of blood vessels as their transport system, travelling through the body rapidly, releasing potent toxins as they go. The immune system launches an all-out attack, but by this point the damage is often too severe. The body is overrun with bacteria, and there is rapid swelling in the brain. Victims face mortality rates of up to 50%, and those who survive are often left with severe after-effects, including deafness and paralysis.

My research focuses on the role of white blood cells, neutrophils, which patrol our bloodstream looking for intruders. They are voracious killers that detect infection and arrive first on the scene, primed for attack. Neutrophils use an arsenal of weaponry to launch the cellular version of chemical warfare. The potent chemicals degrade the bacterial cell, destroy its proteins and attack its DNA, killing the bacterium rapidly.

We know that the meningococcus comes into contact with neutrophils during meningitis, but little is known about what happens when they meet. I study this interaction by extracting neutrophils and infecting them. Usually, bacteria are killed by neutrophils within 30 minutes. However, the meningococcus not only survives, but actually grows inside them.

Neutrophils can cross from the bloodstream into the brain and spinal cord. What if the bacteria hijack the neutrophils for their own gain? Not only would they be able to travel rapidly around the body and cross into the brain, they would be hidden from the rest of the immune system. It would be the ultimate stealth tactic.

My work is exploring how the meningococcus is able to survive in the hostile environment within the neutrophil. I have found that the bacterium possesses a repair system for preventing DNA damage, enabling it to withstand the neutrophils' attack far better than other species. I am also investigating how the meningococcus might use food sources inside the host cell. I believe it is likely that the bacterium scavenges inside the cell, bulking up its defences while simultaneously depriving the neutrophil of its resources.

If we are to tackle meningitis, it is imperative we understand as much about the disease as possible. This is the route towards developing vaccines and improving treatments. If the meningococcus is equipped to injure us by manipulating our defences, we need to retaliate. Through better understanding of the disease, we hope to find more effective ways to fight back.